My dear Adolfo
Where is my one and only Florante?
He's gone
I fed him to the Lions
My loving Princess
Don't cry anymore
Even if Florante left you behind
I'm still here
Adolfo will be loving you now
Now don't cry
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The complement system is an essential and powerful part of our immune defense system.
Its main function is to coordinate the destruction and removal
of infectious organisms, known as pathogens, or damaged cells in our body
that need to be replaced. The complement system consists of a cascade of proteins,
which activate each other by cleavage, the process of splitting each protein
one-by-one. The complement system may be activated by three different pathways
- the alternative, classical, and lectin pathways that all run through Complement
C3, the central protein in the cascade.
C3 serves as the master switch controlling all downstream effectors
that ultimately cause destruction of the cell.
The alternative pathway is spontaneously activated through direct binding of
complement to a pathogen or damaged host cell, to help the body clear away debris.
The classical pathway is activated when an antibody, a protein produced by our
immune system, recognizes and binds to a component on the surface of a foreign
cell, forming an immune complex – starting an immune response that targets the
pathogen for destruction. The lectin pathway is activated by
natural molecules in our body that recognize sugars at the surface of infectious organisms.
In situations where the complement system becomes over activated,
it results in immune attack – the destruction of healthy cells, and
ultimately causes illness to the person.
Paroxysmal nocturnal hemoglobinuria, PNH, is a rare, acquired, potentially
life-threatening blood disorder characterized by chronic, complement-
mediated destruction of red blood cells –hemolysis– and formation of
life-threatening blood clots, also known as thrombosis. In PNH, stem cells acquire
a gene mutation which results in the production of abnormal blood cells.
These defective red blood cells, white blood cells and platelets, lack the connector,
known as GPI, for two important surface proteins–CD55
and CD59–that regulate complement activity.
As a result, the complement protein C3 becomes unregulated, triggering all
downstream effectors that ultimately cause destruction of blood cells.
In intravascular hemolysis, the formation of the membrane attack complex known as MAC,
creates holes in red blood cells causing them to rupture inside blood vessels.
At the same time,...Extravascular hemolysis is caused by C3b
being deposited on the surface of defective red blood cells, tagging them
for removal and resulting in their destruction in the liver and spleen.
Platelets are also susceptible to excessive activation and cell
aggregation resulting from the presence of extra C3a, C5a and MAC, increasing
the risk of developing deadly blood clots.
Current treatment blocks the complement protein C5, which prevents MAC-forming holes on red blood cells
inside blood vessels. However, this does not act upon C3-related extravascular
hemolysis, which continues to cause severe anemia and transfusion dependency
in many PNH patients.
Inhibiting the C3 protein may prevent both intravascular and extravascular hemolysis.
When the complement system becomes over activated, medical treatment is required
to regain control and protect the body from immune attacks .
APL-2 is a PEGylated cyclic peptide inhibitor of complement C3.
PEGylation helps keep APL-2 in the body longer, reducing dosing frequency.
The peptide portion of APL-2 binds to enough C3 to prevent it from completing
the complement cascade...helping the body regain control by preventing excessive
complement activity...and protecting it from abnormal immune attacks.
Multiple global clinical trials are underway to determine if C3 inhibition provides
improved clinical outcomes compared with current standards of care.
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